The Redox–Inflammation Axis in Atherosclerosis and Ischemic Stroke: Mechanisms, Biomarkers, and Translational Challenges

Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide and are driven by the interplay between oxidative stress and chronic inflammation. Although these processes have been extensively investigated, their integration into a unified mechanistic framework and their translational relevance for biomarker-guided precision medicine remain insufficiently addressed. This narrative review integrates mechanistic, biomarker, and translational perspectives on the redox–inflammation axis in atherosclerosis and acute ischemic stroke, critically evaluating oxidative and inflammatory biomarkers while highlighting current challenges and emerging therapeutic opportunities. Reactive oxygen and nitrogen species (ROS/RNS) promote endothelial dysfunction, lipid oxidation, and activation of redox-sensitive pathways, including NF-κB, Nrf2/Keap1, JAK/STAT, and the NLRP3 inflammasome, resulting in vascular inflammation and injury. Biomarkers such as hs-CRP, IL-6, MPO, MDA, F2-isoprostanes, oxLDL, and antioxidant enzyme activity have demonstrated associations with cardiovascular risk, disease severity, and clinical outcomes, and therefore show diagnostic and prognostic potential. However, with the exception of selected inflammatory biomarkers, most oxidative stress biomarkers have not yet been sufficiently validated for routine clinical use because of biological variability, limited specificity, and insufficient analytical standardization. Disappointing outcomes of antioxidant supplementation further reflect the complexity of redox biology and the dual physiological and pathological roles of ROS. Here, we highlight that future progress in cardiovascular medicine will require a shift from non-specific antioxidant supplementation to precision redox modulation, integrating multimarker profiling, system biology, multi-omics, and artificial intelligence and machine-learning approaches to improve cardiovascular risk stratification and personalized therapy.

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Journal
International Journal of Molecular Sciences
Published
2026-07-27
DOI
https://doi.org/10.3390/ijms27156705
Primary Topic
Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Type
article
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0.00

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article

The Redox–Inflammation Axis in Atherosclerosis and Ischemic Stroke: Mechanisms, Biomarkers, and Translational Challenges

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International Journal of Molecular Sciences
Neutrophil, Myeloperoxidase and Oxidative Mechanisms
article

The Redox–Inflammation Axis in Atherosclerosis and Ischemic Stroke: Mechanisms, Biomarkers, and Translational Challenges

Natalia Serwin, Barbara Dołęgowska, Małgorzata Goszka, Aleksandra Polikowska, Elżbieta Cecerska‐Heryć, Rafał Heryć, Adrianna Jerzyk, Cezary Gaczyński, Urszula Łacek
article en

Abstract

Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide and are driven by the interplay between oxidative stress and chronic inflammation. Although these processes have been extensively investigated, their integration into a unified mechanistic framework and their translational relevance for biomarker-guided precision medicine remain insufficiently addressed. This narrative review integrates mechanistic, biomarker, and translational perspectives on the redox–inflammation axis in atherosclerosis and acute ischemic stroke, critically evaluating oxidative and inflammatory biomarkers while highlighting current challenges and emerging therapeutic opportunities. Reactive oxygen and nitrogen species (ROS/RNS) promote endothelial dysfunction, lipid oxidation, and activation of redox-sensitive pathways, including NF-κB, Nrf2/Keap1, JAK/STAT, and the NLRP3 inflammasome, resulting in vascular inflammation and injury. Biomarkers such as hs-CRP, IL-6, MPO, MDA, F2-isoprostanes, oxLDL, and antioxidant enzyme activity have demonstrated associations with cardiovascular risk, disease severity, and clinical outcomes, and therefore show diagnostic and prognostic potential. However, with the exception of selected inflammatory biomarkers, most oxidative stress biomarkers have not yet been sufficiently validated for routine clinical use because of biological variability, limited specificity, and insufficient analytical standardization. Disappointing outcomes of antioxidant supplementation further reflect the complexity of redox biology and the dual physiological and pathological roles of ROS. Here, we highlight that future progress in cardiovascular medicine will require a shift from non-specific antioxidant supplementation to precision redox modulation, integrating multimarker profiling, system biology, multi-omics, and artificial intelligence and machine-learning approaches to improve cardiovascular risk stratification and personalized therapy.

International Journal of Molecular SciencesVol. 27(15)
Pomeranian Medical University (PL)
Pomorski Uniwersytet Medyczny W Szczecinie
Good health and well-being
Openalex Percentile: Top 16%
Neutrophil, Myeloperoxidase and Oxidative Mechanisms
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